Vitamin D and Cardiovascular Health

Abstract

A 56-year-old black female patient with significant coronary heart disease (CHD) after several percutaneous intervention procedures for acute coronary syndromes was seen in the office for routine follow-up. She is 5 ft 5 in tall and weighs 265 pounds. She had recently gained 25 pounds after losing nearly 100 pounds following bariatric surgery. Her blood pressure, which was previously controlled with her therapy for hypertension, which included a β-blocker, an angiotensin-converting enzyme inhibitor, a calcium blocker, and a diuretic, was 160/90 mm Hg. Her fasting glucose was 168 mg/dL, with a hemoglobin A1C of 8.4% on therapy for type 2 diabetes mellitus. She was experiencing severe myalgias, which made it difficult for her to exercise, so she discontinued her atorvastatin. Her fasting lipid profile was as follows: total cholesterol, 264 mg/dL; high-density lipoprotein, 42 mg/dL; triglycerides, 220 mg/dL; and low-density lipoprotein, 178 mg/dL. Her 25-hydroxyvitamin D [25(OH)D] level was severely low at 8 ng/mL. There have been several nutrient fads over recent decades, including beta carotene, selenium, folic acid, and vitamins E and C, all of which failed to show benefit in multiple large, randomized, controlled trials and thus did not stand the test of time, at least in terms of major cardiovascular event reduction.1,2 Without question, vitamin D increases absorption of calcium, magnesium, and phosphorus and mobilizes calcium and phosphorus from bone. It is also clear that vitamin D deficiency adversely affects the musculoskeletal system, predisposing to rickets in children and osteomalacia and osteoporosis in adults. The potential role of vitamin D in the pathogenesis of statin-induced myopathy and myalgias is debatable, although currently it appears reasonable to use vitamin D supplementation in patients with such symptoms, especially if …